Status Asthmaticus

By Adem Lewis / in , , , , , , , , , , , , , , , , , /

Today, we’re going to be talking about status asthmaticus. Status asthmaticus is defined as a form of severe asthma that fails to respond to inhale beta agonist, oral IV steroids, or oxygen. This will usually require the patient being admitted to the hospital for their treatment. Risk factors that are concerning for status asthmaticus from a social standpoint include inner city residents, poor outpatient compliance, and denial of disease severity. Medically, you’re concerned about worsening respiratory failure, specifically rapid sudden deterioration. You do want to inquire about past ICU admission, as well as a prior intubation in the patient. Understanding asthma involves understanding the pathophysiology. This is what I like to call the big three– they include bronchospasm, edema, and mucus production. The mechanics of status asthmaticus involve understanding that asthma is a nonhomogeneous airway disease, not an alveolar disease. The big three cause a decrease in airway diameter, and thus an increase in airflow resistance. During inspiration, negative pleural pressures cause physiological intrathoracic airway dilation. Looking at this schematic, you can see that the patients don’t have an issue bringing air in, as the negative pressure of the thorax allows that. But during expiration, the pleural pressures approach zero, causing physiological intrathoracic airway narrowing. This is seen in this schematic where we see dilation of the alveoli as the air has come in, but because of the inflammation is unable to get out. This process is known as air trapping. So why are these patients breathing so hard? Again, as we saw in our last schematic, there is higher end-expiratory lung volumes. The broncospasm that’s seen with asthma leads to increased airway resistance and reduced expiratory flow. Unlike a patient who is not affected by asthma, expiration is now active, and that is secondary to the air trapping. So as we look at this schematic, we see our big three therefore lead to atelectasis. This atelectasis, which is airway collapse caused by inability of air to get down and out of the bronchials decreases ventilation in the midst of adequate pulmonary blood flow. The results of that process causes hypoxemia, which is decreased oxygenation and shunting of blood in the pulmonary vasculature bed. As our big three worsen, the air trapping and the V/Q mismatch, ventilation perfusion, also worsen, leading to tachypnea and more pronounced atelectasis. During this phase, the hypoxemia that the patient is experiencing can worsen. And as they are trying to increase their respiratory rate to compensate for the air trapping, we can see hypocarbia. Unfortunately, without treatment, these patients will have muscle fatigue and thus increased respiratory effort is unable to compensate for the increased dead space with air trapping and airway distension. This causes worsening hypoxemia and hypocarbia, which will then lead to respiratory failure. As we look at treatment, it is important to acquire IV access. Remember, although we do not want to over-hydrate, under-hydration is also a concern. These patients will have increased insensible losses, and these will need to be compensated for in your management. Ensure that you put these patients on cardiorespiratory monitoring, put a pulse ox on them to ensure that oxygen therapy is being effectively treated. It is always a concern of acquiring a blood gas. And I would encourage you to assess your patient clinically for further deterioration as you look to advance their treatments. Steroids are the mainstay of care for these patients, as its immunosuppressant effects help to decrease inflammatory cells migration to the area of disease. This also has an effect on airway mucus production. Where if your dose of steroids, you should expect to see an effect in one to three hours of treatment, with max effect at 48 hours of treatment. Methylprednisolone is the preferred use of steroids, as it relates to asthma with this limited mineralocorticoid effect. You will see that some institutions also use dexamethasone and hydrocortisone. Although a dose is provided for you, be advised several institutions will use various dosing for their patients. Inhaled beta agonist also coincide with steroids as the mainstay of treatment, as they help to relax the bronchial airways. Salbutamol and levalbuterol are what are most frequently used. The dose is also again dependent upon your institution of care. In severe disease, we will see the use of IV and subcutaneous beta agonists. They also cause direct bronchial smooth muscle relaxation. Terbutaline is one that is commonly used, but care must me minded, as there are reports of myocardial ischemia with this use. In a subcutaneous version, we will also see ephedrine, epinephrine, and isopreterenol used as well. The methylxanthines, theophylline would be an example, promote relaxation of the smooth muscle, as well as pulmonary diuresis. Although this drug has shown positive effects, caution must be used in following levels. Reports of seizure activity had been seen once levels approximate 20 micrograms per milliliter. The anticholinergics, specifically ipratropium bromide, also help promote broncodilation without the inhibition of mucociliary clearance. Studies have shown the use of anticholinergics in the ED setting has significantly improved the decrease in hospital admissions, as well as the patient’s overall clinical asthma score. As with asthma therapy, the combination of therapies have allowed for improvement in care. Theophylline, added to IV beta agonists or inhaled beta agonists, and ipratropium bromide and steroids, although did not reduce the PICU length of stay, they significantly improve the clinical asthma score. Magnesium sulfate, another bronchodilator, again helps with this aspect of status asthmaticus. You will read in reports controversy over its efficacy, but it is frequently used in the care of these patients. The combination of the gas of helium-oxygen helps to reduce the airflow resistance in these small airways, thus improving the patient’s care. Studies have shown that the use of heliox with continuous albuterol therapy in children in the ED with moderate to severe asthma was associated with significant improvement in clinical asthma score. Also, the use of heliox in mechanically ventilated patients helped reduce the peak airway pressure, a concern with moving to mechanical ventilation for these patients. Although antibiotics are not the mainstay of therapy, inquiring in a history for a cause of inciting issues as it pertains to the asthma, specifically atypical pneumonias or a specific bacterial infection like a sinusitis, can help you tailor antibiotic therapy to assist your patients. You will read about using ventilation in these patients with caution. Non-invasive mechanical ventilation has shown promising trials, but there is no definitive data for the use of status asthmaticus. Mechanical ventilation should be reserved for the patient whose clinical appearance shows indicators that the patient may be tiring out without the use of mechanical ventilation will not likely survive. The concerns with mechanical ventilation is that we must remember that asthma is a lower airway disease, and the endotracheal tube does not open to smaller airways. The positive pressure given by mechanical ventilation may also distend to healthier airways, therefore worsening air trapping. Be mindful that mechanical ventilation can have negative effects with cardiac interactions with decreased venous return, the barotrauma that’s seen with high pressures, worsening edema, and even death with the use of this form of therapy. If you are in the presence that you need to intervene, please be mindful to avoid histamine releasing agents, such as those listed below. Medication such as ketamine is a good anesthetic to use because of its broncodilator effects and its ability preserve your hemodynamics. Again, as you look to care for a patient with asthma, remember that you are treating the patient from the aspects of broncospasm, edema inflammation, and mucus production. And therefore, your therapy should be adjusted appropriately.

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